ArticleJournal of neurophysiology2009
Excitatory actions of noradrenaline and metabotropic glutamate receptor activation in granule cells of the accessory olfactory bulb.
Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Article
- Contactin-6-deficient male mice exhibit the abnormal function of the accessory olfactory system and impaired reproductive behavior.Brain and behavior · 2023Article
- The Bruce effect: Representational stability and memory formation in the accessory olfactory bulb of the female mouse.Cell reports · 2022Article
- αFrontiers in cellular neuroscience · 2022Article
- Signal Detection and Coding in the Accessory Olfactory System.Chemical senses · 2018Review
- αLearning & memory (Cold Spring Harbor, N.Y.) · 2018Article
- Experience-Dependent Plasticity in Accessory Olfactory Bulb Interneurons following Male-Male Social Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Heterogeneous effects of norepinephrine on spontaneous and stimulus-driven activity in the male accessory olfactory bulb.Journal of neurophysiology · 2017Article
- Activation of β-noradrenergic receptors enhances rhythmic bursting in mouse olfactory bulb external tufted cells.Journal of neurophysiology · 2016Article
- A targeted genome association study examining transient receptor potential ion channels, acetylcholine receptors, and adrenergic receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis.BMC medical genetics · 2016Article
- Differential Muscarinic Modulation in the Olfactory Bulb.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Disruption of centrifugal inhibition to olfactory bulb granule cells impairs olfactory discrimination.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- α(1A)-Adrenergic regulation of inhibition in the olfactory bulb.The Journal of physiology · 2013Article
- Stressors impair odor recognition memory via an olfactory bulb-dependent noradrenergic mechanism.Frontiers in integrative neuroscience · 2013Article
- Cholinergic modulation of neuronal excitability in the accessory olfactory bulb.Journal of neurophysiology · 2010Article
- Activation of alpha1 and alpha2 noradrenergic receptors exert opposing effects on excitability of main olfactory bulb granule cells.Neuroscience · 2010Article
- Protein kinase Calpha mediates a novel form of plasticity in the accessory olfactory bulb.Neuroscience · 2009Article
- Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Modulation of dendrodendritic synapses by the noradrenergic system in the accessory olfactory bulb (AOB) plays a key role in the formation of memory in olfactory-mediated behaviors. We have recently shown that noradrenaline (NA) inhibits mitral cells by increasing gamma-aminobutyric acid inhibitory input onto mitral cells in the AOB, suggesting an excitatory action of NA on granule cells (GCs). Here, we show that NA (10 microM) elicits a long-lasting depolarization of GCs. This effect is mediated by activation of alpha(1)-adrenergic receptors as the depolarization is mimicked by phenylephrine (PE, 30 microM) and completely blocked by the alpha(1)-adrenergic receptor antagonist prazosin (300 nM). In addition to this depolarization, application of NA induced the appearance of a slow afterdepolarization (sADP) following a stimulus-elicited train of action potentials. Similarly, the group I metabotropic glutamate receptor (mGluR1) agonist DHPG (10-30 microM) also produced a depolarization of GCs and the appearance of a stimulus-induced sADP. The ionic and voltage dependence and sensitivity to blockers of the sADP suggest that it is mediated by the nonselective cationic conductance I(CAN). Thus the excitatory action resulting from the activation of these receptors could be mediated by a common transduction target. Surprisingly, the excitatory effect of PE on GCs was completely blocked by the mGluR1 antagonist LY367385 (100 microM). Conversely, the effect of DHPG was not antagonized by the alpha(1)-adrenergic receptor antagonist prazosin (300 nM). These results suggest that most of the noradrenergic effect on GCs in the AOB is mediated by potentiation of a basal activity of mGluR1s.
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